Axon regeneration failure accounts for permanent functional deficits following neuronal injury in adult mammals. However, the underlying mechanisms that control axon regeneration in the adult CNS and PNS remain elusive. A formidable challenge in neural repair in the adult nervous system is the long distances that regenerating axons often need to travel in order to reconnect with their targets. Thus, a sustained capacity for axon regeneration is critical for achieving functional restoration. Although deletion of either Phosphatase and tensin homolog (PTEN), a negative regulator of mammalian target of rapamycin (mTOR), or suppressor of cytokine signaling 3 (SOCS3), a negative regulator of Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, in adult retinal ganglion cells (RGCs) individually promoted significant optic nerve regeneration, such re-growth tapered off around two weeks after the crush injury1,2. The identification of factors and techniques that promote sustained regeneration to damaged neurons is critical for the development of successful therapeutics.